Medical Pharmacology: Antiarrhythmic Drugs
Practice Questions
Click on the correct answer.
Which one(s) of the following properties are associated with quinidine effects on the heart?
A reduced upstroke velocity of the cardiac action potential
Increased QRS duration as noted on the ECG through blockade of sodium channels
Both
Neither
Toxic cardiac effect(s) as a result of quinidine administration include(s):
Torsades de pointes arrhythmia
Excessive Q-T prolongation as noted on ECG
Both
Neither
Therapeutic uses of quinidine include(s):
Preventing recurring ventricular tachycardia or fibrillation
Maintenance of normal sinus rhythm in patients who had exhibited atrial flutter or atrial fibrillation.
Both
Neither
Cardiac ion currents affected by quinidine include(s):
Sodium current
Cardiac potassium currents
Both
Neither
This cardiac membrane current is more likely affected by quinidine only at higher quinidine concentrations.
Sodium current
Rapid component of the delayed rectifier (IKr)
L-type calcium current
None of the above
Mainly at reduced heart rates, quinidine antagonism of this cardiac ion-channel is responsible for action potential prolongation.
Sodium channels
Potassium channels
Quinidine administration causes both ß-adrenergic receptor blockade and inhibition of vagal nerve activity.
True
False
The most common non-cardiac adverse effect following quinidine administration:
Hepatitis
Lupus syndrome
Thrombocytopenia
Diarrhea
Percentage of patients receiving quinidine treatment will develop significant Q-T-interval lengthening and torsades de pointes arrhythmias.
<1%
2-8%
20-25%
40-50%
Quinidine is a significant inhibitor of the cytochrome P450 drug metabolizing isoform, CYP2D6. Which one(s) of the following activities occur due to quinidine's effect on CYP2D6-mediated metabolism?
Quinidine-inducedi nhibition of CYP2D6 metabolism of codeine to the active form, morphine, decreases the analgesic effect
Quinidine-induced inhibition of CYP2D6 metabolism of propafenone causes higher plasma propafenone levels with increased ß-adrenergic receptor inhibition.
